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W Carter

Publications and source records attributed to W Carter.

49 records · Page 3Linked to original sources
PubMed1979

The CSF pressure-volume relationship before and after cardiac arrest in the cat.

The CSF pressure-volume (P-V) function was evaluated before and after cardiac arrest in 15 cats. The CSF volume change was produced by bolus loading (loading rate, greater than 0.1 mL/s) of the CSF space. Comparison of the CSF P-V function before and after cardiac arrest was made over a CSF pressure range of 5 to 46 mm Hg and for a CSF volume change of up to 9% of total CSF volume. After cardiac arrest, all CSF P-V curves were well described by the mathematical model konwn to be valid under normal physiological conditions. In eight animals, there was no significant difference between the prearrest and postarrest P-V functions. For the seven animals demonstrating a significant difference between prearrest and postarrest P-V data, all but one of the postarrest P-V curves were within the normal range. These results suggest that the shape of the CSF P-V curve is not substantially altered by cardiac arrest. We conclude that under normal circumstances material properties of brain tissue are the most important factors in determining the configuration of the CSF P-V curve and that under normal circumstances cerebral hemodynamic factors do not affect the shape of this curve.

Animals↗
PubMed1979

Bolous versus steady-state infusion for determination of CSF outflow resistance.

For rapid changes in cerebrospinal fluid volume an exponential relationship was demonstrated between CSF pressure and CSF volume in 15 cats. This relationship was valid over a CSF pressure range from 7 to 50 mm Hg and for acute increases of up to 9% to total CSF volume (approximately 13 ml for humans). Our data agree well with previous reports for the cat. A similar relationship has been shown in the dog and in humans. It has been claimed that, given the equations for CSF bulk flow and the exponential relationship between CSF pressure and CSF volume, one can calculate CSF outflow resistance by observing the decay of CSF pressure after a bolus injection into the CSF space. This claim was evaluated in an additional 18 cats. In these animals CSF outflow resistance calculated by the bolus method was compared with resistance calculated by a steady-state infusion method over the CSF outflow resistance range of 74 to 293 mm Hg/ml min-1. Resistance calculated by the bolus method underestimated resistance calculated by the steady-state method, and this underestimate grew larger with increasing resistance. The bolus technique is therefore not a valid method for determining CSF outflow resistance. The explanation offered for these results is that the decay of CSF pressure after a bolus injection into the CSF space occurs not only because of runoff of the injected volume of CSF but also because of "pressure relaxation" of the brain parenchyma around the CSF space. The phenomenon of pressure relaxation was not considered in developing the equation for calculation of CSF outflow resistance by the bolus technique. The time dependency of pressure relaxation allows for a fundamental element of hysteresis within the CSF space. A method of quantifying this element of hysteresis is suggested.

Animals↗
PubMed1979

Repair of chest wall defects with prosthetic material.

This report summarizes our experience during a four-year period with the repair of 8 thoracic cage and 3 diaphragmatic defects requiring reinforcement with prosthetic material. Defects as large as the entire left hemidiaphragm or the right anterior chest wall including ribs two through six from the midsternum to the midaxillary line were adequately repaired. The technical approach utilized to obtain a secure, nonmobile thoracic cage involved the placement of sutures through drill holes or around ribs, rather than through the periosteum or pericostal soft tissues. Successful diaphragmatic repair was dependent on proper anchoring of the medial border of the prosthesis, placing sutures in the pericardium as necessary. Skin coverage for thoracic cage defects was achieved with widely undermined and advanced local tissue or previously delayed pedicle flaps. All patients had good evidence of chest wall stabilization after operation, and all were removed from mechanical ventilation within three days. One patient died of myocardial infarction twenty days after operation, and a second patient died later of metastatic disease. On the basis of our experience, we conclude that the range of chest wall lesions that can be surgically corrected or palliated is increased by the use of prosthetics implanted with techniques described here.

Adult↗
PubMed1976

Re-examination of porcine and bovine hypothalamic fractions for additional luteinizing hormone and follicle stimulating hormone-releasing activities.

More than 150 hypothalamic fractions were reassayed for luteinizing hormone-releasing hormone (LHRH) and follicle stimulating hormone-releasing hormone (FSHRH) activities in search for LHRH and FSHRH which differ from the decapeptide (pyro)Glu-His-Trp-Ser-Try-Gly-Leu-Arg-Pro-Gly-NH2 (I). Among the porcine fractions tested were those obtained: 1) from the isolation of thyrotropin-releasing hormone; 2) from two isolation procedures for LHRH; and 3) from methanolic and aqueous 2N acetic acid extracts which were subjected to Biogel P-2 filtration and partition chromatography. Some bovine hypothalamic fractions were also tested. Both in vivo and in vitro assays were used for measuring LHRH and FSHRH activities. The values obtained were in each case compared with those resulting from the administration of pure natural or synthetic LHRH decapeptide I. A radioimmunoassay for LHRH (I) was also utilized for some fractions. In all the purification steps the location of LHRH and FSHRH activity, as determined by in vivo assays, corresponded to that of the decapeptide I. Purification of hypothalamic extracts on Biogel P-2 and by partition chromatography separated a fraction from the decapeptide I, which released more FSH than LH in vitro from the pituitaries of immature female rats. However, this material was inactive in vivo and in other in vitro systems, so that its significance is obscure. The results suggest that if material with LHRH and FSHRH activity other than the decapeptide I is present in acid extracts of porcine hypothalami, then its FSHRH and LHRH activity would be a minor part of the total LHRH/FSHRH activity in the extracts. (Pyro)-Glu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2 appears to account for most of all of the LHRH and FSHRH activity found.

Animals↗
PubMedDate not supplied

Failure to validate a predictive model for refusal of care to emergency-department patients.

OBJECTIVE: To determine whether previously developed triage criteria for refusal of care to patients presenting to an emergency department (ED) with nonurgent problems could be validated for an independent patient population. METHODS: A convenience sample of 534 adults presenting to a municipal hospital ED between July 1, 1992, and October 15, 1992, who met preestablished criteria for refusal of care were entered into a prospective, observational, cohort study. The single target outcome variable was hospitalization. In order to optimize the criteria's performance, both the triage nurse and the physician caring for the patient had to agree that all criteria for "refusal of care" were specifically met. No patient was refused care, nor was a patient's management or disposition interfered with in any way by the investigators. All patients were followed until hospital admission or release from the ED. RESULTS: Six (1.1%) of 534 patients (95% CI 0.4-2.4) who met the criteria for refusal of care were hospitalized. This represents a greater than 50-fold difference in incidence of hospitalization when compared with that found by other investigators, who reported that only 0.02% (95% CI 0.0004-0.04) of those patients who were refused care subsequently required hospitalization (p < 10 (-7)). CONCLUSION: The authors were unable to validate a previously developed predictive model for refusal of care to patients presenting to an ED. Refusal of care to selected ED patients based on current guidelines is not a viable solution to overcrowding. Alternative strategies must be sought.

Adult↗
PubMedDate not supplied

Evaluating clinical accuracy of systems for self-monitoring of blood glucose.

Although the scientific literature contains numerous reports of the statistical accuracy of systems for self-monitoring of blood glucose (SMBG), most of these studies determine accuracy in ways that may not be clinically useful. We have developed an error grid analysis (EGA), which describes the clinical accuracy of SMBG systems over the entire range of blood glucose values, taking into account 1) the absolute value of the system-generated glucose value, 2) the absolute value of the reference blood glucose value, 3) the relative difference between these two values, and 4) the clinical significance of this difference. The EGA of accuracy of five different reflectance meters (Eyetone, Dextrometer, Glucometer I, Glucometer II, Memory Glucometer II), a visually interpretable glucose reagent strip (Glucostix), and filter-paper spot glucose determinations is presented. In addition, reanalyses of a laboratory comparison of three reflectance meters (Accucheck II, Glucometer II, Glucoscan 9000) and of two previously published studies comparing the accuracy of five different reflectance meters with EGA is described. EGA provides the practitioner and the researcher with a clinically meaningful method for evaluating the accuracy of blood glucose values generated with various monitoring systems and for analyzing the clinical implications of previously published data.

Blood Glucose↗